2023
DOI: 10.1016/j.jaip.2023.02.005
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Targeting Skin Barrier Function in Atopic Dermatitis

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Cited by 29 publications
(8 citation statements)
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“…Skin barrier dysfunction is characteristic finding of AD, substantially contributing to its progression and the manifestation of pruritic symptoms ( Kim and Leung, 2018 ; Leung et al, 2020 ; van den Bogaard et al, 2023 ). Therefore, to understand the mechanisms underlying the positive effects of advanced FOS on AD symptoms, we investigated whether advanced FOS modulates the expression of ELOVL s and epidermal barrier proteins, which are associated with skin barrier function ( Kim and Leung, 2018 ).…”
Section: Discussionmentioning
confidence: 99%
“…Skin barrier dysfunction is characteristic finding of AD, substantially contributing to its progression and the manifestation of pruritic symptoms ( Kim and Leung, 2018 ; Leung et al, 2020 ; van den Bogaard et al, 2023 ). Therefore, to understand the mechanisms underlying the positive effects of advanced FOS on AD symptoms, we investigated whether advanced FOS modulates the expression of ELOVL s and epidermal barrier proteins, which are associated with skin barrier function ( Kim and Leung, 2018 ).…”
Section: Discussionmentioning
confidence: 99%
“…Earlier findings indicate a reduced chain length of FFA and ceramides in atopic skin (nLAS vs. HS and LAS vs. nLAS) [33,80,81], especially the very-long-chain FFA [47,82], which causes decreased formation of the orthorhombic lateral organisation in favour of the less dense hexagonal organisation [33,83,84]. Higher levels of inflammatory cytokines (such as IFN-α) are potential factors causing this reduction in the chain length by decreasing the two elongases of fatty acids ELOVL 1 and ELOVL4 [4,80] and higher IL-4/13 levels inhibiting ELOVL3 and ELOVL6 [40]. Apart from chain length, the level of saturation in FFA also influences the lateral ICL organisation [85], with corresponding differences being observed among LAS, nLAS, and HS regarding the concentration of unsaturated FFA and the activity of the corresponding processing enzymes [80].…”
Section: Discussionmentioning
confidence: 99%
“…Thus, it is not surprising that reduced or even total loss of filaggrin in AD is associated with lower NMF concentration, higher TEWL, skin xerosis [4,37], and higher Staphylococcus aureus colonisation [29]. While genetic filaggrin mutations are not found in all AD patients [38][39][40], inflammatory cytokines such as IL-4/13 are also able to reduce filaggrin expression. Other described factors responsible for the impaired atopic SBF are dysfunctional tight junctions [41], reduced antimicrobial peptides [4], and a disturbed milieu of commensal microbiome [42][43][44], e.g., with reduced presence of physiologically appearing Cutibacterium, Streptococcus, Corynebacterium, and Proteobacteria, in favour of Staphylococcus colonisation [45] which correlates with higher TEWL [46].…”
Section: Introductionmentioning
confidence: 99%
“…Although parents may desire to identify underlying causes to AD, there is typically no underlying etiology identified for AD in an individual child. Even prior to visible manifestation of AD, sampling of the skin microbiome by noninvasive self-adhesive skin tape strips identified indicators of more severe AD, including colonization with Staphylococcus aureus (SA), higher levels of interleukin (IL)-13 and thymic stromal lymphopoietin (TSLP) in the epidermis at two months of age, increased transepidermal water loss at three months of age, and increased levels of the chemokine, CCL17, two months prior to the appearance of AD [2 ▪▪ ,3 ▪ ,4].…”
Section: Risk Factors For Atopic Dermatitismentioning
confidence: 99%